[Are there pulmonary vascular or respiratory effects of prostaglandin vehicles (ethanol, glycine buffer) after intravenous infusion or inhalation?]. / Verursacht die Infusion oder Inhalation von Prostaglandin-Trägerlösungen (Athanol, Glycin-Puffer) pulmonalvaskuläre oder respiratorische Effekte?

BACKGROUND: Infusion or inhalation of prostaglandins PGE1 and PGI2 is used to reduce vascular resistance. PGE1 and PGI2 are dissolved in ethanol and glycine buffer, respectively. Each vehicle may cause dose-dependent haemodynamic and respiratory side effects. This study was performed to examine the role of low-dose ethanol and glycine buffer as used for the infusion and inhalation of PGE1 and PGI2. METHODS: Two groups of pigs (ethanol and glycine group, n = 9 each) were anaesthetised and ventilated mechanically. Ethanol was given at 0.14 mg/kg/min by infusion and 0.12 mg/kg/min as aerosol, glycine buffer was infused at 3.8 microg/kg/min and inhaled at 3.1 microg/kg/min, respectively. Haemodynamic and respiratory data were recorded before and after application. RESULTS: Neither infusion nor inhalation of ethanol or glycine buffer caused significant changes in systemic and pulmonary haemodynamics, right heart function, oxygenation or ventilation. CONCLUSIONS: The effect of inhaled or intravenously infused PGE1 and PGI2 is not influenced by their preparations containing ethanol or glycine buffer.

Pressure-controlled versus volume-controlled one-lung ventilation for MIDCAB.

One-lung ventilation is limited by hypoventilation and hypoxemia because of increasing airway pressure and intrapulmonary shunt. Previous clinical studies compared pressure-controlled versus volume-controlled ventilation during one-lung ventilation in patients with pre-existing pulmonary disease. We studied 50 patients undergoing thoracotomy and one-lung ventilation because of cardiovascular disease. After two-lung ventilation with volume-controlled ventilation, patients were divided randomly into two groups. In one group, ventilation was switched to pressure-controlled ventilation after starting one-lung ventilation. In the other group, volume-controlled ventilation was continued. Parameters of ventilation, pulmonary function and systemic and pulmonary hemodynamics were recorded. We observed, that peak airway pressure, dead space ventilation and arterial carbon dioxide partial pressure were significantly higher during volume-controlled ventilation. After one-lung ventilation patients with pressure controlled ventilation had lower alveolar-arterial oxygen tension difference and a higher arterial oxygen partial pressure with significant differences for those patients in the intensive care unit. We conclude that pressure-controlled ventilation may be useful to improve gas exchange and alveolar recruitment during one lung ventilation.

Cardiopulmonary effects of intravenous prostaglandin E1 during experimental one-lung ventilation.

BACKGROUND: One-lung ventilation greatly improves operating conditions during thoracic surgery. Serious disadvantages of one-lung ventilation are hypoxaemia and increased pulmonary vascular resistance. Prostaglandins, like prostaglandin I2 (PGI2), are potent pulmonary vasodilators but may also influence venous admixture and systemic circulation. Since the lung is capable of extensive degradation of prostaglandin E1 (PGE1) but not of PGI2, PGE1 might affect systemic circulation to a lesser degree. Hence, we studied the effects of intravenous PGE1 on systemic and pulmonary circulation and on oxygenation during one-lung ventilation. METHODS: Lateral thoracotomy and cross-clamping of the left main stem bronchus was performed in twelve anaesthetised and ventilated pigs. Animals were cannulated with arterial, central venous and fast response thermodilution pulmonary artery catheters for haemodynamic measurements. PGE1 was administered with infusion rates of 25, 50, and 100 ng x kg (-1) x min (-1) during one-lung ventilation. RESULTS: All doses of PGE1 significantly decreased pulmonary vascular resistance and mean pulmonary artery pressure. However, a comparable significant reduction in systemic vascular resistance and mean arterial pressure was found. Arterial oxygen tension and venous admixture showed a slight but significant deterioration. Oxygen delivery remained unchanged or increased since the cardiac index increased. CONCLUSION: During one-lung ventilation in the pig, infusion of PGE1 significantly decreased pulmonary vascular resistance and pulmonary artery pressure but failed to achieve selective pulmonary vasodilation.

[Complications due to patient positioning: anaesthesiological considerations]. / Lagerungsschäden aus der Sicht des Anästhesisten.

Anaesthetist and surgeon cooperate in positioning the patient for surgery according to interdisciplinary agreements. The legal demands on documentation for standard positioning procedures are met with a symbol or short notice on the anaesthesia protocol. In the case of damage to the patient, however, the doctor has to furnish evidence that the patient has been positioned correctly. Complications associated with perioperative patient positioning are reported to be 1 to 1000. Peripheral nerves are at highest risk, but soft tissue, joint, vascular and ocular damages are also reported. The problems and adequate care of different positioning modes, such as recumbent, lateral, prone, seated and lithotomy position, are discussed in detail.

[Aerosolized and intravenous prostacyclin during one-lung ventilation. Hemodynamic and pulmonary effects]. / Inhalatives und intravenöses Prostazyklin während der Ein-Lungen-Ventilation. Hämodynamische und pulmonale Effekte.

BACKGROUND: One-lung ventilation is frequently used in thoracic surgery. However, hypoxic pulmonary vasoconstriction of the atelectatic lung may produce pulmonary hypertension. The objective of the present study was to compare the acute effects of intravenous versus aerosolized prostacyclin (PGI(2)) on pulmonary and systemic circulation. METHODS: PGI(2) was administered in 11 anesthetized and unilaterally ventilated pigs by infusion (5, 10, and 20 ng/kg body weight/min) and by inhalation (4, 8, and 16 ng/kg body weight/min) in a cross-over design. RESULTS: Infusion of PGI(2) reduced both pulmonary (PVR) and systemic vascular resistance (SVR). Due to a concomitant increase in cardiac index (CI) mean arterial (MAP) and pulmonary artery pressures (MPAP) did not change significantly. In contrast, aerosolized PGI(2) produced a significant decrease in PVR (-21.4 to -32.8%) and MPAP (-12.0 to -17.8%) without affecting SVR, MAP, and CI. Arterial oxygenation tension (p(a)O(2)) was not affected. CONCLUSION: During one-lung ventilation only aerosolized prostacyclin produced a selective pulmonary vasodilation.

Inhaled nitric oxide as a prophylactic treatment against reperfusion injury of the lung.

BACKGROUND: Inhaled Nitric Oxide (NO) has been found to be effective in clinical treatment of reperfusion injury after lung transplantation. This study was designed to determine a possible prophylactic role to reduce severe reperfusion injury. METHODS: In 12 minipigs the left lung was selectively perfused with cold Euro-Collins solution. After 90 minutes of warm ischemia the lungs were reperfused and the contralateral pulmonary artery and main bronchus clamped. Hemodynamic and respiratory parameters were monitored for 7 hours. 6 animals were used as controls. 6 pigs formed the NO group and were ventilated continuously with 40 ppm nitric oxide (NO) starting 30 minutes prior to reperfusion. RESULTS: In the control group right heart failure developed within 1.9 +/- 0.8 hours of reperfusion. Lung compliance was significantly reduced. A significant increase of pulmonary vascular resistance (PVR) was found. All animals of the NO group survived the reperfusion period of 7 hours. PVR was decreased compared to controls (p = 0.03). AaDO2 was lower, but not significantly different. The dynamic compliance of the lung was significantly higher (p = 0.007) in the NO group. CONCLUSIONS: The prophylactic institution of inhaled NO reduces reperfusion injury of the lung. Short-term use of inhaled NO should be adopted as a prophylactic agent after transplantation of lungs preserved in Euro-Collins solution.

Inhaled nitric oxide and inhaled prostaglandin E1: effect on left ventricular contractility when used for treatment of experimental pulmonary hypertension.

OBJECTIVE: Pulmonary hypertension (PHT) is a life-threatening complication after isolated heart and lung transplantation. Recent work has shown that inhaled nitric oxide (NO) in combination with inhaled prostaglandin E1 (PGE1) reduce pulmonary hypertension but their influence on cardiac contractility is less well defined. METHODS: This study investigated left ventricular contractility as measured by the 'Preload Recruitable Stroke Work-Relation' (PRSW) in 24 anesthetized open chest pigs, 12 receiving in random order NO (50 ppm), PGE1 (20 microg/ml) and their combination compared to 12 controls. PHT was induced by embolization with glass beads (500 microm). Prior to induction of PHT, sonomicrometric crystals were placed on the heart to measure instantaneous cardiac dimensions. Instantaneous intraventricular pressure (micro-tip catheter) and intraventricular dimensions were recorded digitally, while intraventricular volumes were calculated from the intraventricular dimensions applying the cylindric ellipsoidal volume model for the left ventricle. PRSW was calculated from the instantaneous pressure and volume data during rapid vena caval occlusion by analysis of generated pressure-volume loops. All data were analyzed by MANOVA and corrected for heart rate (level of significance #: P < 0.05); PRSW-slope measures contractility, (PRSW-X-intercept did not change significantly). RESULTS: PRSW-change +/- SEM (in percent of initial PRSW after induction of PHT) was -14.6% +/- 4.4% versus 1.6% +/- 4.4% for NO versus Control (P = 0.004), -8.8% +/- 4.6% versus 1% +/- 3.3% (P = 0.18) for PGE1 versus Control and -5.7% +/- 4.4% versus 2.5% +/- 4.2% for NO + PGE1 versus Control (P = 0.33), respectively. In summary, application of NO 50 ppm significantly reduced left ventricular contractility while PGE1 20 microg/ml and the combination of NO and PGE1 did not. CONCLUSION: If NO is not available, the sole application of nebulized PGE1 (20 microg/ml) appears to be safe with respect to left ventricular contractility in the setting of PHT. The combination of NO and PGE1 for the treatment of pulmonary hypertension should be considered for clinical application in situations where a combination of pulmonary hypertension and decreased left ventricular function is present.

Remifentanil, fentanyl, and alfentanil have no influence on the respiratory burst of human neutrophils in vitro.

BACKGROUND: Anaesthetic agents inhibit certain functions of human neutrophils. The respiratory burst (RB) enzyme in the plasma membrane of neutrophils leads to the production of superoxide anion. The oxygen radicals are responsible for killing phagocytised micro-organisms. We investigated the in vitro influence of remifentanil, fentanyl, and alfentanil on the respiratory burst of human neutrophils. METHODS: For the flow-cytometric evaluation, leukocytes were obtained as supernatant following sedimentation and were incubated with the tested drugs. The concentrations in vitro were adjusted to conform to the plasma concentrations reported for anaesthesia and also to 10-fold higher concentrations. The RB was measured by intracellular oxidation of dihydrorhodamine to fluorescent rhodamine after induction of phorbol-myristate-acetate (PMA), Escherichia coli (E. coli) or priming by tumour necrosis factor alpha followed by stimulation of n-formyl-methionyl-leucyl-phenylalanine (TNF-alpha/FMLP). In order to exclude prestimulation of the neutrophil granulocytes, negative controls were carried out. Propidium iodide (PI) was added for viability discrimination immediately prior to flow cytometry measurement. RESULTS: Regardless of the triggering agents chosen (PMA, E. coli, TNF-alpha/FMLP), remifentanil, fentanyl, and alfentanil had no significant effect on the neutrophils' respiratory burst even in concentrations which were higher than those encountered during in vivo conditions. CONCLUSION: With respect to peri- and postoperative risk of infection, anaesthetics and analgetics with no inhibiting effect on neutrophil function should be used. These results show that remifentanil, fentanyl, and alfentanil do not influence the neutrophils' respiratory burst in vitro.

Effect of lung allograft ischaemia duration on postreperfusion graft function and postoperative course.

Lung transplantation is limited by the effects of ischaemia. Previous clinical studies related graft ischaemia duration to post-operative pulmonary function in the ICU, morbidity, and overall survival. This report describes the intraoperative pulmonary allograft function immediately after reperfusion. 23 lung transplantations (15 bilateral, 8 single) were analysed. Donor selection and organ procurement were identical. After pulmonary vasodilation with prostacyclin, allografts were flush-perfused with cold modified Euro-Collins solution. Mean duration of lung ischaemia was 255.1 +/- 35.1 min (190-314 min). Ischaemia times did not differ with respect to the recipient's disease or the use of extracorporeal circulation. After reperfusion, oxygenation indices deteriorated in 73.9% of patients compared with the native lungs (313.4 +/- 163.5 vs 427.2 +/- 96.1, p = 0.006). Linear regression analysis and subgroup analysis both revealed a significant influence of the duration of allograft ischaemia on early transplant function. Ischaemia of more than 4 hours resulted in an acceptable but significantly lower PaO2 (254.9 +/- 143.3 mmHg vs 463.0 +/- 149.2 mmHg, p = 0.011). However, mean time until extubation and time spent in the ICU were not affected. It is concluded that flush-perfusion of the lung with modified Euro-Collins solution provides reliable preservation of lung function up to four hours. Longer ischaemia, up to six hours, is followed by an acceptable but progressively reduced early transplant function.

Monitoring of respiratory function before and after cardiopulmonary bypass using side-stream spirometry.

Pulmonary impairment is more frequent after cardiac surgery than after other major surgical procedures. The present study investigates whether, by using standard respiratory monitoring, i.e. side-stream spirometry and blood gas analysis, it is possible to detect changes in pulmonary function secondary to cardiopulmonary bypass. We investigated 18 patients undergoing elective coronary bypass surgery or aortic valve replacement. Cardiopulmonary bypass resulted in a nonsignificant increase in alveolar-arterial oxygen difference from 33.0 +/- 10.6 kPa to 36.1 +/- 12.5 kPa and arterial to end-tidal CO2 tension difference from 0.67 +/- 0.39 kPa to 0.79 +/- 0.54 kPa. Respiratory system resistance was unaltered. In contrast, dynamic compliance decreased significantly after cardiopulmonary bypass from 78.6 +/- 22.9 to 65.4 +/- 22.4 mL cmH2O-1 with open chest and from 61.0 +/- 10.2 to 51.1 +/- 17.2 mL cmH2O-1 with closed chest, compared with corresponding values before cardiopulmonary bypass. In conclusion, pulmonary gas exchange was not compromised after cardiopulmonary bypass, but a diminished respiratory compliance was a consistent finding, even in uncomplicated cardiac surgery using routine respiratory monitoring.

A tube in the pharynx for emergency ventilation.

BACKGROUND: If the endotracheal placement of a nasal advanced tube fails, ventilation via this tube could bridge the time until a fibreoptic bronchoscope is available. This study investigates the efficiency of ventilation via a tube resting with its tip in the pharynx near the glottis. METHODS: In 20 patients respiratory data during ventilation via a pharyngeally placed tube were recorded by means of pulse oximetry, capnometry and side-stream spirometry. Results were compared with those measured previously in the same patients during conventional facemask ventilation. RESULTS: Oxygen saturation and end-tidal carbon dioxide concentration remained unchanged using ventilation via facemask (SO2 98.5 +/- 0.9%, FECO2 4.5 +/- 0.7 vol%) or pharyngeal tube (SO2 98.6 +/- 0.7%, FECO2 4.8 +/- 0.4 vol%). No significant differences were found between the two groups with regard to peak airway pressure, tidal volume leakage, compliance and resistance of the respiratory system. CONCLUSIONS: Our results suggest an effective ventilation and oxygenation via a tube placed with its tip in the pharynx. This technique may be helpful during difficult and prolonged nasal intubation.

[Ventilation via a transnasally placed pharyngeal tube. Comparison with mask ventilation]. / Ventilation über einen transnasal im Pharynx plazierten Tubus. Vergleich mit der Maskenbeatmung.

OBJECTIVE: The present prospective study was designed to investigate the respiratory function during ventilation via a tube inserted through the nose into the pharynx. Results were compared with respiratory parameters measured during conventional mask ventilation in the same patients. METHODS: 20 ASA physical status I-II patients were studied after approval by the local Ethics Committee. Anaesthesia was induced with alfentanil 15 micrograms/kg and propofol 2.5-3.0 mg/kg and maintained with propofol, 12-15 mg/kg/h. Patients were ventilated via a facemask with oxygen and a tidal volume of approximately 8ml/kg (measurement A). After insertion of a tube (I.D. 7.0-7.5 mm) through the nostril into the pharynx ventilation was repeated in the same manner (measurement B). To secure airway seal a second person closed the patient's mouth and exerted cricoid pressure. Following neuromuscular blockade with suxamethonium (1.5 mg/kg) respiratory parameters were measured again (C). Measurements included pulse oximetry and side stream spirometry with continuous collection of the following data: airway pressure, inspired and expired tidal volume, dynamic compliance, expired volume in one second, inspiratory and expiratory oxygen and carbon dioxide concentration. Pressure-volume and flow-volume loops were displayed continuously. RESULTS: Ventilation via facial mask or via pharyngeal tube with and without relaxation showed normal endtidal FECO2. The mean values were 4.5 +/- 0.7%, 4.8 +/- 0.4% and 4.6 +/- 0.7%, respectively. Mean oxygen saturation exceeded 98% in each period. Leakage during mask ventilation was 59.3 +/- 65.5 mL and decreased to 40.5 +/- 62.1 mL with the pharyngeal tube, whereas relaxation resulted in a significant increase to 92.3 75.0 mL. Compliance (Cdyn) and expired volume in one second (V 1.0) did not change significantly during the entire period of measurement. CONCLUSION: The use of a pharyngeally placed tube proved adequate compared to conventional mask ventilation in 20 patients without underlying airway disease.

[Is preventive perioperative dopamine administration of value?]. / Ist die prophylaktische perioperative Dopamingabe sinnvoll?

Dopamine interacts in a dose dependent manner with three types of receptors: the alpha- and beta-adrenoceptors and specific dopaminergic receptors. Hence dopamine can exert direct and indirect renal effects. Stimulation of myocardial beta 1-receptors causes an increase in cardiac output and a subsequent augmentation of renal blood flow. However, a major role of selective renal vasodilation in response to dopamine has been brought into question by recent studies. In addition, dopamine has been shown to decrease tubular transport of sodium and to produce sodium diuresis. This natriuresis may induce volume depletion with further deterioration of renal function. Expectations that low-dose dopamine could have a renal-sparing potential did not prove true. Prophylactic infusion of low-dose dopamine in patients undergoing aortic surgery, orthotopic liver grafting or renal transplantation failed to show a renal protective effect or an improved clinical outcome. The routine use of "renal-dose" dopamine therefore cannot be recommended. More attention must be paid to prevent or abolish prerenal causes of renal impairment. Basic measures as volume expansion, care of cardiocirculatory status and close monitoring of renal function are of special importance.

[Combined lung and liver transplantation. Anesthesiologic management]. / Kombinierte Lungen- und Lebertransplantation. Anästhesiologisches Management.

A 53-year-old man with alpha-1-antitrypsin deficiency had an 8-year history of progressive dyspnoea and two episodes of bleeding oesophageal varices with liver decompensation. After the diagnosis of terminal pulmonary emphysema (Fig. 1) and liver cirrhosis with progressive liver failure was made, he was accepted for combined lung and liver transplantation. METHODS. Anaesthesia was induced with thiopentone and fentanyl and maintained with fentanyl, midazolam, and isoflurane. After relaxation with succinylcholine, the patient's trachea was intubated with a left endobronchial double-lumen tube. Haemodynamic monitoring included arterial, central-venous, pulmonary-artery, and capillary-wedge pressures and cardiac output measurement. Ventilatory monitoring consisted of pulse oximetry, side-stream spirometry, and continuous measurement of arterial and mixed-venous blood oxygen saturation with fibreoptic catheters. A left single-lung transplantation was performed under one-lung ventilation without cardiopulmonary bypass. Prostacyclin was infused to reduce pulmonary vascular resistance. The transplant was ventilated separately with 50% oxygen and positive end-expiratory pressure of 8-10 cm H2O, and then liver transplantation was carried out. The institution of veno-venous bypass during the anhepatic phase failed because of portal-vein and axillary-vein thrombi. RESULTS. Total operation time was 6 h 30 min. Clamping of the left pulmonary artery lasted 45 min and the duration of the anhepatic phase was 92 min. Ventilation and oxygenation during lung transplantation caused no problems (Table 1). Clamping of the left pulmonary artery caused a slight increase in pulmonary vascular resistance (104 to 124 dyn.s.cm-5) and mean pulmonary artery pressure (25 to 27 mm Hg) without a decrease in cardiac index (Table 2). During the anhepatic phase with exclusion of the portal vein and inferior vena cava, a marked decrease in cardiac index (-27.2%) was seen (Table 4). The operation required substitution with 10 units packed red blood cells, 12 units fresh frozen plasma, and 5 platelet concentrates. The post-operative course showed normal liver graft function (Table 5). Acute pulmonary rejection on the 7th day was treated successfully with methylprednisolone. The patient's trachea has extubated 10 days after transplantation and he was discharged from the intensive care unit 2 weeks later. CONCLUSION. The management of this combined lung and liver transplantation was performed according to the experience with isolated lung and liver transplants in our hospital. Aggressive haemodynamic and ventilatory monitoring, including systemic and pulmonary arterial fibreoptic catheters, seems of particular importance in such high-risk procedures.

[Photoplethysmography evaluation of collateral blood flow before puncture of the dorsalis pedis artery]. / Photoplethysmographische Kollateralflussprüfung vor Punktion der A. dorsalis pedis.

Prior to cannulation of the dorsalis pedis artery the collateral circulation through the plantar arch should be examined to evaluate the consequence of an occlusion of this artery. Since the performance of the Allen's test is impossible for assessment of the plantar arch, another suitable technique has to be chosen. We selected the photoelectric plethysmography. Toe pulses were recorded with photoelectric plethysmography in 20 neurosurgical patients. The pulse amplitudes were measured before and during successive compression of the dorsalis pedis and the posterior tibial artery. Obvious decrease or absence of the pulse wave during compression of the dorsalis pedis artery is indicating an inadequate collateral circulation and cannulation of this artery seems not to be safe. In our study this occurred in 4 of 32 examined feet (12.5 percent). The photoelectric plethysmography has proved to be a simple and accurate means for assessment of collateral circulation.